Cardiac systolic dysfunction in past illicit users of anabolic androgenic steroids / Jon Jarløv Rasmussen, Morten Schou, Per L. Madsen, Christian Selmer, Marie L. Johansen, Peter S. Ulriksen, Tina Dreyer, Thomas Kümler, Louis L. Plesner, Jens Faber, Finn Gustafsson, Caroline Kistorp. - (American Heart Journal (2018) 203 (September) ; p. 49-56).
- PMID: 30015068.
- DOI: 10.1016/j.ahj.2018.06.010
Abstract:
Background
Illicit use of anabolic androgenic steroids (AAS) is associated with left ventricle (LV) systolic dysfunction and increased LV mass (LVM), but whether these findings persist in former AAS users has yet to be elucidated. The objective was to assess LV systolic function, LVM and myocardial fibrosis in current and former illicit AAS users compared with non-users.
Methods
Community-based cross-sectional study among men, aged 18–50 years, involved in recreational resistance training. We included 37 current and 33 former illicit AAS users, geometric mean (95%CI), 30 (21; 44) months since AAS cessation, and 30 non-users as controls. We assessed myocardial function and structure using advanced echocardiography and cardiac MRI with late-gadolinium enhancement.
Results
Mean (SE) LV global longitudinal strain (GLS) was impaired in former AAS users compared with non-users, −16.7 (0.5) versus −18.2 (0.4) %, P < .05. Mean (SE) LV ejection fraction (EF) was decreased, 51 (1) versus 58 (1) %, P < .001 and LV GLS impaired, −14.5 (0.4)%, P < .001, in current AAS users compared with non-users. Measures of LVM were increased in current AAS users compared with the other two groups, P < .001. Plasma total testosterone was independently associated with reduced LVEF (P = .049) and increased LVM/body surface area (P = .005) in multivariate linear regressions. Focal myocardial fibrosis was not detected in any participants and diffuse myocardial fibrosis, assessed using post-contrast T1-mapping time, did not differ among the three groups.
Conclusions
Past illicit AAS use is associated with impaired LV GLS, suggesting subclinical cardiac systolic dysfunction years after AAS cessation.
